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Cardiac sympathectomy promote anti-inflammatory response by activating JAK2-STAT3-mediated signaling cascade in rat myocarditis model: a novel mechanism with clinical implications

Other Titles
 쥐 심근염 모델에서 심장교감신경절제술을 통한 JAK2-STAT3 신호전달 활성화에 따른 항염증 효과 
Authors
 박혜림 
Issue Date
2017
Abstract
Introduction: Left stellectomy has become an important therapeutic option for patients with potentially fatal arrhythmias. However, the antiarrhythmic mechanism of left stellectomy is not well known. Cholinergic anti-inflammatory pathway (CAIP) is a complex immune mechanism that regulates peripheral inflammatory responses. This study evaluated the effect of left stellectomy on CAIP using rat experimental autoimmune myocarditis (EAM) models. Methods: EAM was produced by injecting 2 mg of porcine cardiac myosin into the footpads of rats. Left stellectomy was performed before EAM induction. We evaluated the effect of left stellectomy on arrhythmic events, survival, inflammation and CAIP in rats without and with EAM. Results: Left stellectomy prevented arrhythmia and improved survival in EAM rats. Left stellectomy decreased TNF-α, IL-6, and HMGB1 levels (P<0.05 versus EAM) in serum and heart tissues from EAM rats. Serum level of acetylcholine decreased in EAM rats, and increased after left stellectomy in EAM rats. The ratios of phosphated-STAT3/STAT3 and phosphate-JAK2/JAK2 decreased in cell lysates of spleen, liver and heart in EAM rats. However, the same ratios significantly increased after left stellectomy. NF-κB in cell lysates of spleen, liver, and heart increased in EAM rats, but decreased after left stellectomy. Conclusions: In EAM models, left stellectomy increased survival of the rats while showing antiarrhythmic effects with reduced inflammation via activation of JAK2-STAT3-mediated signaling cascade. Our findings suggest an exciting opportunity to develop new and novel therapeutics to attenuate cardiac inflammation.
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Appears in Collections:
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 5. Others
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/175092
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